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Titolo:
Inhibition of heart mitochondrial lipid peroxidation by non-toxic concentrations of carvedilol and its analog BM-910228
Autore:
Santos, DJSL; Moreno, AJM;
Indirizzi:
Univ Coimbra, Ctr Neurosci, Coimbra, Portugal Univ Coimbra Coimbra Portugal Coimbra, Ctr Neurosci, Coimbra, Portugal Univ Tras os Montes & Alto Douro, Vila Real, Portugal Univ Tras os Montes & Alto Douro Vila Real Portugal Vila Real, Portugal Univ Coimbra, Dept Zool, Coimbra, Portugal Univ Coimbra Coimbra Portugal niv Coimbra, Dept Zool, Coimbra, Portugal
Titolo Testata:
BIOCHEMICAL PHARMACOLOGY
fascicolo: 2, volume: 61, anno: 2001,
pagine: 155 - 164
SICI:
0006-2952(20010115)61:2<155:IOHMLP>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAT-LIVER MITOCHONDRIA; BETA-ADRENOCEPTOR ANTAGONIST; FREE-RADICALS; MYOCARDIAL-ISCHEMIA; ENDOTHELIAL-CELLS; OXIDATIVE STRESS; ALPHA-TOCOPHEROL; MEMBRANE; REPERFUSION; ANTIOXIDANT;
Keywords:
carvedilol; BM-910228; heart mitochondria; antioxidants; lipid peroxidation; oxidative stress; reactive oxygen species;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
52
Recensione:
Indirizzi per estratti:
Indirizzo: Moreno, AJM Univ Coimbra, Ctr Neurosci, Coimbra, Portugal Univ Coimbra Coimbra Portugal r Neurosci, Coimbra, Portugal
Citazione:
D.J.S.L. Santos e A.J.M. Moreno, "Inhibition of heart mitochondrial lipid peroxidation by non-toxic concentrations of carvedilol and its analog BM-910228", BIOCH PHARM, 61(2), 2001, pp. 155-164

Abstract

Carvedilol, a non-selective beta -adrenoreceptor blocker, has been shown to possess a high degree of cardioprotection in experimental models of myocardial damage. Reactive oxygen species have been proposed to be implicated in such situations, and antioxidants have been demonstrated to provide partial protection to the reported damage. The purpose of our study was to investigate the antioxidant effect of carvedilol and its metabolite BM-910228 bymeasuring the extent of lipid peroxidation in a model of severe oxidative damage induced by ADP/FeSO4 in isolated rat heart mitochondria. Carvedilol and BM-910228 inhibited the thiobarbituric acid-reactive substance formation and oxygen consumption associated with lipid peroxidation with IC50 values of 6 and 0.22 muM, respectively. Under the same conditions, the IC50 values of alpha -tocopheryl succinate and Trolox were 125 and 31 muM, respectively. As expected, the presence of carvedilol and BM-910228 preserved the structural and functional integrity of mitochondria under oxidative stress conditions for the same concentration range shown to inhibit lipid peroxidation, since they prevented the collapse of the mitochondrial membrane potential (Delta psi) induced by ADP/FeSO4 in respiring mitochondria. It should bestressed that neither carvedilol nor BM-910228 induced any toxic effect onmitochondrial function in the concentration range of the compounds that inhibits the peroxidation of mitochondrial membranes. In conclusion, the antioxidant properties of carvedilol may contribute to the cardioprotective effects of the compound, namely through the preservation of mitochondrial functions whose importance in myocardial dysfunction is clearly documented. Additionally, its hydroxylated analog BM-910220, with its notably superior antioxidant activity, may significantly contribute to the therapeutic effects of carvedilol. (C) 2001 Elsevier Science Inc. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/04/20 alle ore 12:12:10